Regulatory T cells (Tregs) fulfill a central role in immune regulation. We reported previously that the integrin αEβ7 discriminates distinct subsets of murine CD4+ regulatory T cells. Use of this marker has now helped to unravel a fundamental dichotomy among regulatory T cells. αE −CD25+ cells expressed L-selectin and CCR7, enabling recirculation through lymphoid tissues. In contrast, αE-positive subsets (CD25+ and CD25−) displayed an effector/memory phenotype expressing high levels of E/P-selectin–binding ligands, multiple adhesion molecules as well as receptors for inflammatory chemokines, allowing efficient migration into inflamed sites. Accordingly, αE-expressing cells were found to be the most potent suppressors of inflammatory processes in disease models such as antigen-induced arthritis.

Peroral infection with Toxoplasma gondii leads to the development of small intestinal inflammation dependent on Th1 cytokines. The role of Th17 cells in ileitis is unknown. We report interleukin (IL)-23–mediated gelatinase A (matrixmetalloproteinase [MMP]-2) up-regulation in the ileum of infected mice. MMP-2 deficiency as well as therapeutic or prophylactic selective gelatinase blockage protected mice from the development of T. gondii–induced immunopathology. Moreover, IL-23–dependent up-regulation of IL-22 was essential for the development of ileitis, whereas IL-17 was down-regulated and dispensable. CD4+ T cells were the main source of IL-22 in the small intestinal lamina propria. Thus, IL-23 regulates small intestinal inflammation via IL-22 but independent of IL-17. Gelatinases may be useful targets for treatment of intestinal inflammation.

Severe acute respiratory syndrome coronavirus 2 infection and development of coronavirus disease 2019 presents a major health care challenge of global dimensions. Laboratory diagnostics of infected patients, and the assessment of immunity against severe acute respiratory syndrome coronavirus 2, presents a major cornerstone in handling the pandemic. Currently, there is an increase in demand for antibody testing and a large number of tests are already marketed or are in the late stage of development. However, the interpretation of test results depends on many variables and factors, including sensitivity, specificity, potential cross-reactivity and cross-protectivity, the diagnostic value of antibodies of different isotypes, and the use of antibody testing in identification of acutely ill patients or in epidemiological settings. In this article, the recently established COVID-19 Task Force of the German Society for Clinical Chemistry and Laboratory Medicine (DGKL) addresses these issues on the basis of currently available data sets in this rapidly moving field.

Objective. To visualize early experimental arthritis with near-infrared fluorescence (NIRF) imaging in a murine model of antigen-induced arthritis (AIA).Methods. The target of NIRF was the F4/80 antigen present on the surface of macrophages infiltrating the inflamed synovial membrane. Imaging was performed using anti-F4/80 monoclonal antibodies (mAb) labeled with Cy5.5 fluorochrome. On day 7 of AIA, 6 mice received an intravenous (IV) injection of labeled mAb; control AIA mice (n ‫؍‬ 6) received an IV injection of Cy5.5-labeled isotype control antibody. NIRF imaging was performed before injection (baseline) and until 72 hours thereafter. Histologic evaluation of arthritis severity and immunohistochemical assessment of F4/80 antigen density were also performed on day 7.Results. NIRF imaging showed an accumulation of fluorochrome probes in the inflamed knee joints and, to a lesser extent, in the contralateral (nonarthritic) knee joints. The signal induced by mAb F4/80 was clearly higher than that generated by the isotype control. Accumulation of fluorochrome probes in the joints was confirmed histologically by confocal laser scanning microscopy.Conclusion. The use of fluorochromes allows imaging of arthritis in the near-infrared range. Accumulation in the contralateral, nonarthritic knee joints can be explained by the presence of sentinel macrophages in normal synovium or by a mild contralateral response due to systemic activation or neurogenic mechanisms.